Alterations of the hormone-receptors on or within cells will modify the response of target tissues to various hormones thus serving to control cellular growth or function. We have shown that the number of detectable prolactin receptors is controlled in vivo by the circulating levels of prolactin or growth hormone by a positive feedback mechanism. Inhibition of in vivo prostaglandin (PG) synthesis by either enzymatic blockade or precursor depletion results in a loss of existing PRL receptors and prevents their induction by PRL. As membrane fluidity increases in a variety of hormonal, dietary or developmental states, the number of PRL receptors also increases. This has been shown in vitro to be achieved by PGI2 over a very narrow concentration range. It has also been demonstrated that PRL alters PG synthesis in vivo. These data suggest that PRL up-regulates its own receptor by modifying target membrane fluidity and that this may occur through modification of prostaglandin synthesis. These studies have been extended to the DMBA rat mammary tumor, with the regressing tumor membranes more viscous than those of the growing tumor. An assay for PG receptor has been developed.